Inverse agonism of cannabinoid CB₁ receptors potentiates LiCl‐induced nausea in the conditioned gaping model in rats

Abstract

Inverse agonism, but not neutral antagonism, of CB(1) receptors potentiated toxin-induced nausea. This effect may be peripherally mediated or may be mediated centrally by action on CB(1) receptors, located distal to the cerebral ventricles.